At ULCA, researchers conducted a study that tested women who regularly consumed yogurt containing the beneficial bacteria probiotics if they had any alteration in brain function compared to women who did not eat yogurt. The study showed that the women who ate the yogurt regularly had an alteration of brain function in both a resting state and in a series of tests for recognizing emotions. Researchers speculated that by changing the bacteria’s environment in the gut could result in changes in the functionality of the brain. The study was small, 36 healthy women from ages 18-55. The women were divided into three groups: one group was given yogurt with probiotics twice a day for four weeks, one group was given yogurt that was a look-alike yogurt with no probiotics, and the third group did not have any yogurt. MRI scans done before and after the study to compare the results of the brain’s functionality, researchers found that the women who consumed the probiotics yogurt saw a decrease in the insula, which processes and integrates internal processes, as well as in the somatosensory cortex during the emotional-recognition testing. The women also had a decrease in the widespread network of the brain, dealing with emotion, cognition, and sensory-related areas, while the women who did not eat the probiotic yogurt had increased levels of activity. Furthermore, during the resting brain scan, the probiotic women had a higher connectivity in the brain to cognition, while the women not eating any yogurt saw increase of emotional and sensation activity, and the women on the look-alike yogurt fit between the two extremes. Researchers were astounded to find the various brain effects, such as sensations and not just simply emotional responses. The linkage of signals between the intestines and the brain will lead scientists to explore new routes of research in various changes in diet to test for varying levels of brain response and functionality.

Researchers at the University of California, San Diego School of Medicine led a study in which rats were injected with one dose of human neural stem cells which produced improvement of function and mobility, as well as neuronal regeneration in the rats that had an acute spinal cord injury. According to Dr. Martin Marsala, MD, professor of Anesthesiology with colleagues at the University of California, grafting neural stem cells that were derived from a human fetal spinal cord and transferring them to the rats spinal injury site had many therapeutic benefits, ranging from less spasticity of muscles to new connections between the injected stem cells and surviving neurons within the rats. The scientists reported that the human stem cells seemed to take root vigorously at the injury site, aiding the recovery process along to the point where any cavities or cysts that formed at the injury site would disappear when grafted cells were injected. The rats received the stem cells exactly three days after sustaining the spinal injury, in addition to several drugs that lessened the immune response of the rats so that their bodies would properly accept the stem calls. The stem cells appeared to stimulate the rat’s neuron regeneration, as well as partially replacing functionality of lost neurons. The rats had greater control of their paws, and overall would now have a much greater quality of life. With this knowledge in hand, scientists are working to develop neural precursor cells that could potentially become any one of the three cell types found in the nervous system, leading to induced pluripotent stem cells, which when taken from the patient would aid greatly in the process of spinal injury procedures and treatments. Sources:1) Sebastiaan van Gorp, Marjolein Leerink, Osamu Kakinohana, Oleksandr Platoshyn, Camila Santucci, Jan Galik, Elbert A Joosten, Marian Hruska-Plochan, Danielle Goldberg, Silvia Marsala, Karl Johe, Joseph D Ciacci, Martin Marsala. Amelioration of motor/sensory dysfunction and spasticity in a rat model of acute lumbar spinal cord injury by human neural stem cell transplantation. Stem Cell Research & Therapy, 2013; 4 (5): 57 DOI: 10.1186/scrt2092) University of California - San Diego (2013, May 27). Stem cell injections improve spinal injuries in rats. ScienceDaily. Retrieved May 28, 2013, from http://www.sciencedaily.com¬ /releases/2013/05/130527231843.htm

A new study by researchers at the Albert Einstein School of Medicine dramatically underscores the potential role of the NF-kB protein in aging. NF-kB is a master protein which controls many inflammatory chemicals throughout the body. Researchers at the Roskamp Institute have studied NF-kB for many years as a potential way of controlling chronic inflammation which accompanies aging and underlies conditions such as Alzheimer’s disease. This new study points to a part of the brain as regulating the aging process. The current view of aging generally suggests that enzymes, DNA, proteins and other constituents of the body essentially “wear out” with age, accumulating damage due to environmental insults until they no longer function properly. This new study suggests something quite different, namely that a part of the brain called the Hypothalamus deliberately induces aging throughout the body. It has been suggested that one reason why the brain might take such drastic action is to inhibit reproduction past a certain age. This suggestion is highly speculative at this stage, but the data offered by the Albert Einstein researchers suggests that, with age, increased NF-kB activity triggers degeneration in both the brain and other areas of the body. The researchers showed that as mice aged, they increasingly expressed NF-kB in the part of the brain that is normally responsible for the production of reproductive and growth hormones. The researchers artificially manipulated NF-kB activity using genetic techniques and showed that reducing NF-kB activity was associated with better performance in cognitive tests, greater muscle strength and greater bone mass and skin thickness. Conversely, exacerbation of NF-kB activity increased all of these peripheral signs of aging, as well as reducing cognitive abilities. Furthermore the research suggested that microglia (the inflammatory cells resident in the brain) are the originators of the NF-kB activity and this spreads to nearby neurons, including those responsible for growth and reproductive hormones. These findings are of direct significance to work at the Roskamp Institute as researchers there have shown that increased NF-kB collates strongly with Alzheimer’s pathology and pathology of other central nervous system disorders. Moreover, they have worked extensively on ways to reduce NF-kB activation, particularly using the naturally occurring compound Anatabine. Roskamp Institute researchers have shown in multiple preclinical studies of neuroinflammation (such as Alzheimer's, traumatic brain injury and Multiple Sclerosis) that Anatabine (supplied by RockCreek Pharmaceuticals) has potent anti-inflammatory properties. This new finding suggests that NFKB inhibitors might also have a role in decelerating aging. In fact, preliminary studies at the Roskamp Institute suggest that mortality in mice with Alzheimer pathology is reduced by Anatabine treatment. Additional studies are needed to clarify whether Anatabine might reduce the Hypothalamic inflammation and increase the release of hormones that oppose aging.

A study at Emory University School of Medicine has marked another step towards developing an effective blood test for Alzheimer’s disease. This study will be published in the August 28 issue of the journal, Neurology. William Hu, MD, PhD and assistant professor of Neurology at the university was the lead author of hits study; collaborators from University of Pennsylvania and Washington University, St. Louis, were also involved.

Six hundred participants from these institutions took part in the study; these participants were either healthy or diagnosed with Alzheimer’s disease (AD) or mild cognitive impairment (MCI). MCI can be a precursor to Alzheimer’s. The scientists measured the levels of 190 proteins in the blood of the participants. Results indicated that 17 proteins were present in significantly different levels in the blood of those with AD or MCI compared to the healthy volunteers. The researchers checked these 17 proteins with data from another 566 people in the multicenter Alzheimer’s Disease Neuroimaging Initiative. From this, they distinguished four proteins (apolipoprotein E, B-type natriuretic peptide, C-reactive protein, pancreatic polypeptide) that correlated with AD and MCI. In an analysis that clustered people into three groups (MCI, high risk of developing AD, and full AD), it was found that changes in blood levels of these foru proteins are linked to levels of beta-amyloid in the cerebrospinal fluid. Beta-amyloid is the protein that is believed to cause Alzheimer’s when accumulated in the brain.

While there is a way to go, these biomarkers give hope that a blood test for Alzheimer’s can be possible.

Many clinical trials for Alzheimer's Drug failed recently. Dimebon (Latrepirdine) is one of them.

The drug latrepirdine, known as Dimebon, has been featured in two studies previously published in the journal Molecular Psychiatry.The second study showed that latrepirdine could serve as treatment for Alzheimer’s disease, Parkinson’s, as well as other neurodegenerative conditions.

Led by researchers from Mount Sinai School of Medicine, the drug was tested in three different systems (yeast cells, mice cells, and mammal cells), and each system had an accumulation of alpha-synuclein, a protein that causes neurodegeneration. In all three systems, latrepirdine was able to trigger autophagy, a homeostatic process by which the cells break down their own components. The autophagy decreased the amount of synuclein that built up in the mice’s brains.

In the first study, the researchers found that the drug, by activating autophagy, was able to stop the accumulation of beta-amyloid in the brains of mice with Alzheimer’s disease, and their memories also improved. In addition, it was found that the yeast cells were protected by latrepirdine from the toxicity of alpha-synuclein.

Latrepirdine was approved by Russia in 1983 to be sold as an antihistamine in the country. After being effective in treating animal models with Alzheimer’s disease in the 1990s, it underwent a large Phase II clinical trial in Russia with results showing that it significantly improved cognitive function in Alzheimer’s patients with minimal side effects and was able to maintain that improvement. A Phase III clinical trial was carried out in the United States, but there was so sign of improvement in the Alzheimer’s patients. Scientists now believe that the trial failed “because of a lack of understanding of how latrepirdine works”.

Currently, the researchers are seeing if the drug can help treat or prevent Parkinson’s disease, Lewy body dementia, etc, all of which are disorders related to high levels of alpha-synuclein.

A recent study suggests that consuming cocoa flavanols as part of a regulated diet could improve cognitive function. This study, conducted by researchers at the University of L’Aquila in L’Aquila, Italy, was published on August 14 in Hypertension.

Flavanols are a class of flavonoids (plant secondary metabolites with medicinal properties) that are abundant in teas, berries, apples, grapes, red wine, and chocolate. Flavanols can work as an antioxidant. This study involved 90 elderly participants with mild cognitive impairment (MCI), a condition that increases the risk of developing Alzheimer’s or some other form of dementia. The 90 patients were each randomized to consume a dairy-based cocoa flavanol drink of different amounts (990 milligrams, 520 milligrams, or 45 milligrams) for eight weeks. Their diet was cut off of other sources of flavanols. After eight weeks, they participated in neuropsychological tests, and results showed that those in the groups who drank higher levels of cocoa performed significantly higher in the tests than those who drank lower levels of cocoa. Those given the drinks with higher flavanol content also had decreased insulin resistance, blood pressure, and oxidative stress. The decreased insulin resistances levels contributed to 40 percent of the higher results in the cognitive tests.

However, the researchers acknowledge that this was just a small preliminary study that requires larger long-term studies before the results can be confirmed. They still need to determine the amount of cocoa flavanols needed to obtain the benefits and how long these benefits will last. While flavanols has the potential to help improve cognitive function as part of a healthy diet, it is discouraged that people should consume chocolate everyday because of this study.

With the increased life expectancies, the number of the elderly over the age of 90 is rising worldwide. A paper published in the journal, Neurology, focused on a specific study of dementia rates in the very old. Performed in California with over 900 participants, it has shown that there are differences based on gender in risks of dementia or Alzheimer’s disease (AD) for men and women over the age of 90. For women, the chances of developing dementia double by five year increments after 90 years of age, which confirmed the fact that women over 90 are at a greater risk of dementia than men in the same age group. In dementia populations over 90 years of age, only 28 percent of men have dementia, whereas 45 percent of women suffer from the disease. However, the study has revealed that women who had consistently used their brains during their life and had received a higher education had less of a chance of developing dementia compared to those who did not have that benefit. The knowledge that women are at a greater risk than men in developing heart disease or stroke with age, both of which act as independent risk factors for dementia and intensify the symptoms of AD, may be beneficial in understanding why women over 90 are at more risk. In addition, research has shown that Alzheimer’s is also negatively affected by vascular factors, as the work Roskamp Institute scientists’ showed that vasculature damage increases in presence of amyloid. Vascular risk factors are found more frequently in women as they age, and patients in the earlier stages of AD receive a greater neurological impact than normal individuals from vascular damage. Roskamp Institute scientists are using these pieces of information along with other knowledge in order to develop new treatments for dementia.

For more details on this study, as well as additional information on Alzheimer’s disease, please visit

The Roskamp Institute researchers are in search of new treatments for traumatic brain injury (TBI) to help out the veterans of the country. An article in the New England Journal of Medicine has called attention to the number of medical aftereffects of TBI in the American soldiers returning from Iraq. This was revealed through a survey of more than 2,500 soldiers returning from Iraq. Five percent of them stated that they suffered injuries with loss of consciousness, while ten percent said they had injuries that resulted in changed mental status, and another seventeen percent reported other injuries during their deployment. Of the five percent who reported loss of consciousness and of the ten percent who reported altered mental status, 45 percent and 27 percent met the criteria for Post Traumatic Stress Disorder (PTSD), respectively.

The conclusion of the article revolved around the close link between mild TBI, experienced by the veterans from Iraq, with PTSD and physical health problems three to four months after the soldiers come home. In addition, both PTSD and depression serve as mediums for the relationship between mild TBI and physical health issues.

TBI initiates degenerative pathways; researchers at Roskamp are using this knowledge to discover which genes and proteins are connected with these pathways to seek for new treatments for TBI.

For the original article, please visit http://www.roskampinstitute.us/articles/archives/27.

Pro-inflammatory cytokine production can be beneficial to the human body, as it is part of the body’s biological response. However, overproduction of these proteins promotes the development of many deteriorating neurological diseases, such as Alzheimer’s disease (AD) and the neurological damages that are aftereffects of traumatic brain injury (TBI) and stroke. High levels of pro-inflammatory cytokines inhibit proper synaptic communication and function, which eventually leads to damages in the cortex and hippocampus of the brain.

In a study from Northwestern’s Feinberg School of Medicine and University of Kentucky, a new set of drugs have been developed that targets this issue by preventing the overproduction. These drugs target neuroinflammation, a type of brain inflammation that is believed to be a major factor in the injurious nature of diseases ranging from Alzheimer’s to Parkinson’s, as well as brain injuries. The drugs, currently represented by MW151 and MW189, have been tested in previous animal studies. MWI151 was given to a six-month old (the time at which the level of pro-inflammatory cytokines being to increase) mice that are genetically engineered to develop AD for three times a week; then, their brains were examined at eleven months of age, the time at which the conditions of AD are visible. The development of the full-blown AD was avoided as the level of cytokines had returned to normal levels and their synapses were working properly. Mice that were not given the drug still had high levels of pro-inflammatory cytokines and had synaptic malfunction. In another cases, it has also helped decrease the nerve damage caused by TBI by preventing overproduction of pro-inflammatory cytokines and blocking the activation of glia cells. Success was also met when the drug was tested in mice to prevent the development of multiple sclerosis.

Phase one of the first human clinical trial has been completed, but these current studies have shown that the therapy time window is limited, so for future clinical trials, further studies involving models of other diseases and time windows will be conducted. With this new development, the future of early therapy to prevent the development of neurological diseases and the long-term complications of TBI and strokes seems promising.

With Alzheimer’s disease (AD) being the most common type of dementia among the 35 million patients suffering from dementia cases worldwide, the battle to find a drug to at least slow down this disease is becoming more urgent each day. While current medicines do ease the symptoms of AD, none of them delay, stop, or reverse the cognitive and behavioral decline of AD. In recent news, a drug called bapineuzumab, that hoped to improve the cognitive and life functions of the patients participating in the trial, has failed its first of four clinical trials. The 1,100 patients in this late-stage study have mild to moderate cases of Alzheimer’s, and each has a variation of the gene, ApoE4, which increases the chances of developing AD. About half of AD patients have this gene. Bapineuzumab is an antibody based drug that targets beta-amyloid, a protein which scientists believe to be the cause of AD. The failure of this trial may be due to the high risk patients, as well as the fact that the drug is being tested too late into the disease. Jointly created by Pfizer and Johnson & Johnson, it has been announced that Johnson & Johnson will carry out the remaining three clinical trials, with one involving ApoE4 and the other two with patients without the gene. The results of these remaining trials will be presented at a neurology conference in Sweden this September. For more details and news about this study as well as Alzheimer’s disease, please visit: